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Immunology Flashcards

1
Q

what reaction is allergy

A

type 1 hypersensitivity

IgE mediated

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2
Q

what is atopy

A

genetic tendency to produce specific IgE abs on exposure to common environmental antigens

tendency to develop IgE sensitisation

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3
Q

what allergic sx do food allergies produce

A

oral itching, tingling, hives
bronchospasm, wheezeing, laryngeal oedema
anaphylaxis

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4
Q

what happens in a type 1 hypersensitivity reaction

A

IgE attaches to Fc epsilon receptors on mast cells

cross linkage of bound specific IgE by allergen -> degranulation of mast cells and the release of inflammatory mediators

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5
Q

what are the pre-formed mediators in mast cell degranulation

A

histamine
tryptase
heparin
rapid release

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6
Q

what are the synthesised mediators in mast cell degranulation

A

leukotrienes
prostaglandins
slow release

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7
Q

how else can mast cells be activated

A

direct binding of radiocontrast dye, opiates to mast cell

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8
Q

what are the 3 cardinal features of acute allergic reactions and what mediates this

A

pruritus
vasodilation and leakage of fluid = hives, angioedema, hypotension
smooth muscle contraction = bronchospasm

HISTAMINE (acts on histamine receptors)

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9
Q

before planning allergy tests what is required for diagnosis of allergy

A

detailed clinical hx

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10
Q

what are the 2 methods of allergy testing

A

skin prick testing

blood tests - allergen specific IgE in serum

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11
Q

contraindications for skin prick testing

A

severe eczema
unable to stop antihistamines
on immune modulatory drugs
young children

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12
Q

what does a positive result mean in the skin prick tests and blood test

A

only confirms IgE sensitisation - may or may not be associated with clinical allergy (sx)

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13
Q

what are the blood test results for allergy measured in

A

kUA/L

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14
Q

what test must not be used as a screening test for allergy?

A

serum total IgE

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15
Q

why is serum tryptase useful for allergy testing

A

marker of mast cell degranulation
high levels after anaphylaxis
has a short half life - blood needs to be taken ASAP

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16
Q

if tryptase levels are chronically elevated what does this indicate

A

mastocytosis

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17
Q

what is the gold standard for allergy testing

A

double bind placebo control challenge

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18
Q

what is the basophil activation test

A

in vitro assay -activate patient basophils upon exposure to allergen and measure with flow cytometry

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19
Q

what is a true food allergy

A

IgE mediated de-granulation of mast cells.

Common food allergens: cow’s milk protein, egg, peanuts, tree nuts, fish, prawns

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20
Q

what is oral allergy syndrome

A

due to cross reacting ‘pan-allergens’ which are found in various members of the plant family (fruits, vegetables, nuts etc).

They are heat labile and destroyed by digestion, hence symptoms are usually limited to the oral cavity.

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21
Q

what is a false food allergy and what causes it

A

direct stimulation of mast cells or histamine ingestion Scombroid fish poisoning (scombrotoxicosis) – Histamine is released by bacterial action (spoilage) on scombroid fish (e.g tuna). Symptoms that mimic an allergic reaction occur
when the spoiled fish containing histamine is consumed.

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22
Q

what is food intolerance

A

adverse reaction to food, with no histamine related symptoms e.g Lactose intolerance, gluten sensitivity

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23
Q

investigations for suspected food allergy

A

base them on clinical hx

specific IgE blood tests or skin prick tests

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24
Q

what is eczema caused by

A

chronic skin condition
associated with filaggrin gene mutations
leads to poor barrier function of skin -> allows IgE sensitisation to aero-allergens and food allergens because of the thinner epidermis

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25
Q

what factors flare up eczema

A

microbes - infections
irritants - chemicals and soap
allergens - esp aero-allergens
other - temp, foods, stress

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26
Q

if someone has a true food allergy and eczema what can happen

A

eczema can flare up hours after allergic reaction

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27
Q

what is chronic spontaenous urticaria? (CSU)

A

common condition referred inappropriately to the Allergy clinic for ‘allergy testing’

characterised by the spontaneous occurrence of hives (urticaria), swellings (angioedema) or both, with daily or almost daily symptoms for at least 6 weeks

NOT IgE mediated

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28
Q

how is CSU diagnosed?

A

appearance and description of skin lesions with detailed clinical history

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29
Q

what causes CSU?

A 
mast cell degranulation due to 
acute or chronic infections 
stress 
autoimmunity 
pseudo allergy to food and drugs
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30
Q

what makes CSU worse

A

Infections
• Stress
• Alcohol, caffeine, spices, food additives
• Hot showers, hot baths, overheating (duvets in bed)
• Tight clothing
• Medications Aspirin, Paracetamol, NSAIDS, ACE inhibitor, NB: Herbal/natural products
• Soaps, detergents, household products, skin creams and lotions

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31
Q

what is autoimmunity

A

breakdown in the mechanisms that maintain ‘self tolerance’ (elimination of self reactive cells)

leads to activation of self reactive clones of B and T cells

leads to generation of autoantibodies

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32
Q

do healthy individuals produce autoantibodies

A

yes - they help to remove products of tissue breakdown and clear up cell debris

low titre ANA are seen in absence of overt disease

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33
Q

what are autoimmune diseases

A

occurs when humoral and/or cell mediated responses to self antigen are associated with pathological changes

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34
Q

what are the 2 types of autoimmune diseases

A

organ specific

non-organ specific

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35
Q

examples of organ specific autoimmune diseases

A 
MS 
Hashimoto's, thyroiditis, thyrotoxicosis
myasthenia gravis 
pernicious anaemia 
Addison's disease 
insulin dependent DM
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36
Q

examples of non-organ specific autoimmune diseases

A

dermatomyositis
SLE
scleroderma
rheumatoid arthritis

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37
Q

what is autoimmune serology

A

identification and measurement of serum autoantibodies for diagnostic purposes

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38
Q

what are the methods of identification for autoantibodies

A

immunofluorescence, ELISA

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39
Q

what can a positive ANA test indicate

A

connective tissue disease - SLE, Sjorgen’s, sclerosis

rheumatoid arthritis and autoimmune thyroid disease

chronic infectious diseases (mononucleosis, hep C, bacterial endocarditis, TB)

drugs - hydralazine, isoniazid, anticonvulsives

40
Q

what disease is associated with IgA Endomysial antibodies, IgA tTG antibodies

A

coeliac disease

41
Q

what condition are Anti-glomerular basement membrane (GBM) Antibodies associated with

A

Goodpasture’s syndrome

42
Q

what disease is associated with Anti-gastric parietal cell antibodies and Anti-intrinsic factor antibodies

A

pernicious anaemia

43
Q

what antibodies is microscopic polyangitis associated with

A

Anti-MPO (p-ANCA)antibodies

44
Q

what antibodies are phospholipid syndrome (Hughes) associated with

A

anti-cardiolipin antibodies

45
Q

what conditions has Anti SSA (Ro) & Anti SSB(La) antibodies

A

Sjorgen’s syndrome

46
Q

what antibodies are associated with rheumatoid arthritis

A

Anti- cyclic citrullinated peptide (CCP) antibodies (not rheumatoid factor)

47
Q

clinical presentation of Sjogren’s/Sicca syndrome

A 
female (50) 
decrease in secretions 
dry itchy irritated eyes 
dry mouth 
dental problems due to lack of saliva 
difficulty swallowing 
joint pain 
muscle aches 
low mood 
irritability 
impaired concentration 
fatigue
48
Q

clinical presentation of SLE

A

skin (photosensitivity, rashes), joints (pain and swelling often affecting small joints) and organs (including kidneys, lungs, and brain)

49
Q

clinical presentation of phospholipid syndrome

A 
can occur in SLE patients 
high risk of blood clots 
recurrent miscarriages 
arterial/venous thrombosis 
livedo reticularis 
thrombocytopenia
50
Q

clinical presentation of coeliac disease

A 
diarrhoea 
abdominal pain 
bloating 
flatulence 
associated with type 1 DM
dermatitis herpetiformis (blistering on elbows)
51
Q

clinical presentation of myasthenia gravis

A

muscle weakness, commonly affecting muscles controlling the eyes and eyelids, facial expression, chewing, swallowing, and speaking

MG may also affect muscles of the arms, legs, neck, and respiratory muscles

52
Q

antibodies associated with granulomatosis with polyangitis (GPA or Wegener’s granulomatosis)

A

Anti-PR3 (c-ANCA) antibodies

53
Q

clinical presentation of GPA or wegener’s granulomatosis

A

flu like sx (prodromal syndrome associated with ENT problems)
followed by renal failure

54
Q

what are primary systemic vasculitides

A

group of clinical disorders characterised by inflammation of blood vessels causing ischaemia and organ damage

commonly multi system involvement - as inflammation can involve several vascular beds -> renal failure, pulmonary haemorrhage

55
Q

what investigations are ordered for suspected vasculitis

A 
blood test
biopsy
angiography 
antibody tests - ANCA, GBM
serum cryoglobulins 
complement
56
Q

what are the large vessel vasculitis?

A

Giant cell arteritis

Takayasu arteritis

57
Q

what are the medium vessel vasculitis?

A
  • Polyarteritis nodosa

* Kawasaki disease

58
Q

how can small vessel vasculitis be categorised

A

ANCA associated vasculitis

immune complex small vessel vasculitis

59
Q

what are the ANCA associated small vessel vasculitis

A

Granulomatosis with Polyangiitis (GPA) formerly Wegener’s Granulomatosis
Microscopic Polyangiitis (MPA)
Eosinophilic Granulomatosis with Polyangiitis (EGPA) formerly Churg- Strauss syndrome

60
Q

what are the immune complex small vessel vasculitis

A
  • Anti-GBM disease (Goodpasture’s syndrome)
  • Cryoglobulinaemic vasculitis
  • IgA vasculitis (Henoch-Schonlein)
  • Hypocomplementaemic urticarial vasculitis
61
Q

which is the most common small vessel vasculitis

A

Granulomatosis with Polyangiitis (GPA) -formerly ‘Wegener’s granulomatosis

62
Q

what are the 2 forms of granulomatosis with polyangitis

A

generalised form - pulmonary involvement may manifest as breathlessness; renal involvement manifests as (crescentic) glomerulonephritis

localised form - limited to the upper respiratory tract with chronic sinusitis, nasal crusting and/or recurrent epistaxis

63
Q

what is the purpose of immunology testing

A

aids in clinical diagnosis
severity of disease
prognosis of disease
monitoring - disease activity, treatment, relapse, remission

64
Q

what detection method is used for ANA testing

A

immunoflourescne or ELISA

65
Q

what additional tests do you perform after positive ANA test

A

abs to DNA by ELISA (confirms ds-DNA) = crithidia test

abs to ENA - SSA (R0), SSB (La), RNP, Sm, Scl-70, Jo-1

66
Q

what are the 2 classes of immune deficiency?

A

primary and secondary

67
Q

what is primary immune deficiency due to

A

an immunological defect (usually genetic)

very rare

68
Q

what is secondary immune deficiency due to

A 
another disease
drugs - immunosuppresssants, chemo, steroids 
myeloma, CLL
nephrotic dyndrome 
AIDS
protein losing enteropathy
69
Q

what cells make up the innate immune system

A

neutrophils
macrophages
complement

70
Q

what cells make up the adaptive immune system

A

B cells and antibodies

T cells

71
Q

list 5 examples of primary immune deficiency

A 
common variable immune deficiency (CVID)
C1 esterase inhibitor deficiency/hereditary angioedema (HAE)
X-linked agammaglobulinaemia (XLA)
severe combined immune deficiency (SCID)
chronic granulomatous disease (CGD)
72
Q

what are the 6 hallmarks of primary immune deficiency (not HAE)

A 
recurrent 
serious 
unusually persistent 
resistant to treatment 
unusual organisms 
unusual spread
73
Q

what are the 10 warning signs of primary immunodeficiency

A
  1. > =4 new ear infections within 1 year
  2. > = 2 serious sinus infections within 1 year
  3. > = 2 months of abx with little/no affect
  4. > =2 pneumonias per year
  5. failure of infant to gain weight or grow normally
  6. recurrent, deep skin or organ abscesses
  7. persistent thrush in mouth or elsewhere on skin after 1 year of age
  8. requires IV abx to clear infections
  9. > =2 deep seated infections
  10. fhx of primary immune deficiency
74
Q

what pathogens would we expect to see in a T cell defect?

A

pneumocystis
severe fungal/viral infections
HIV

75
Q

what pathogens would we expect to see in a B cell or complement defect?

A

encapsulated bacteria
strep pneumoniae
haemophilius influenzae

76
Q

what pathogens would we expect to see if neutrophils were defective

A

staph
serratia
klebiseilla
aspergillus

77
Q

what pathogens would we expect to see if there was complement deficiency only

A

recurrent neisserial infections

meningitis, gonorrhoea

78
Q

what are patients with primary immune deficiency more predisposed to?

A

autoimmune diseases (deficiency in one section can lead to overactivity in another)
malignancies
granulomatous disease

79
Q

what are the 2 complications of diagnosing a primary immune deficiency late

A

1) irreversible structural damage which can be prevented by early treatment (bronchiectasis, give IV Ig)
2) life threatening laryngeal oedema which can be prevented by appropriate treatment (C1 esterase inhibitor deficiency = hereditary angioedema)

80
Q

what are the initial screening tests for PID?

A

FBC - total lymphocyte and neutrophil count

Serum Igs - IgG, IgA, IgM

Complement - C3 & C4

81
Q

what additional tests can be offered after initial screening and history for suspected PID

A

Specific antibodies to tetanus, haemophilius, pneumococcus (vaccine levels)

Lymphocyte subsets (T cells - CD4, CD8) , B cells, NK cells

C1 esterase inhibitor

NBT test for neutrophil oxidative burst

82
Q

how would someone with common variable deficiency present

A

problem with abs made - require Ig replacement therapy

young adult - male or female

recurrent bacterial infections affecting lungs, sinuses, ears

has autoimmune diseases - idiopathic thrombocytopenic purpura, autoimmune haemolytic anaemia

possible signs of end organ damage such as bronchiectasis

83
Q

what screening test would you request for CVID and what result would you expect

A

serum immunoglobulins

low IgG, low IgA and low/normal IgM

84
Q

what other tests could be requested for suspected CVID diagnosis

A

IgG subclasses

antibodies to haemophilius

lymphocyte phenotyping - normal B and T cells

normal lymphocyte functioning

85
Q

how does X-linked agammaglobulinaemia present

A

affects male infants only (as passed on by mother)

Recurrent bacterial infections of lungs, ears, gut

86
Q

what are the typical results we would expect to see in someone with X-linked agammaglobulinaemia

A

low IgG, IgA, IgM

low total lymphocyte count

low/absent B lymphocytes - problem with the B cells (as very low Igs)

normal T lymphocytes

BTK gene mutations

87
Q

what is severe combined immunodeficiency

A

paed medical emergency

B and T cell disorder

88
Q

what is the typical presentation for SCID

A

young infant/baby

faltering growth

diarrhoea

severe candidiasis (fungus)

89
Q

what results would you expect to see in a SCID patient

A

lymphocyte levels undetectable

both B and T cell very low

low Igs

90
Q

what age do children get their full levels of Igs?

A

2 years

IgG can be higher though as get them through the placenta from mother and breast milk

91
Q

what is hereditary angioedema and what is it a deficiency in

A

autosomal dominant condition associated with low plasma levels of the C1 inhibitor

leads to uncontrolled release of bradykinin resulting in oedema of tissues

C1 esterase inhibitor deficiency

there is a defect in complement (innate immune system) - complement has inhibitors as powerful system

lack of C1 inhibitor leads to complement always being switched on -> low C4 (being used up)

92
Q

what is the clinical presentation for someone with suspected hereditary angioedema

A

recurrent, episodic, non-pitting circumscribed oedema (no urticaria) - often mistaken for anaphylaxis in A&E

unpredictable acute attacks at any body location - face, larynx, tongue, GIT, GUT, hand or arm, leg or foot

93
Q

what screening tests would you order for hereditary angioedema and what would the results be

A

complement components C3 & C4

low C4, normal C3

then confirm by requesting C1 esterase inhibitor (see low levels)

94
Q

what is the treatment for hereditary angioedema

A

C1 esterase inhibitor by infusion

95
Q

what is chronic granulomatous disease

A

defects in proteins involved in oxidative burst of neutrophils/phagocytes (lack of NADPH oxidase)

96
Q

what is the typical presentation for chronic granulomatous disease

A

recurrent pneumonias

recurrent abscesses due to bacteria and fungi (s aureus, aspergillus, klebsiella)

delayed healing

leads to oesophageal strictures (see on barium swallow)

97
Q

what test results would we order for chronic granulomatous disease and what results would we expect

A

FBC - low Hb, normal lymphocytes, elevated neutrophils, elevated ESR

Serum Igs elevated

Raised CRP

Normal neutrophil phagocytosis

Absent neutrophil respiratory burst

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